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目的 :从亚细胞水平研究未成熟心肌缺血 -再灌注损伤中肌浆网 (SarcoplasmicReticulum ,SR)摄钙功能。方法 :36只家兔随机分为 4组 ,进行离体心灌注。组Ⅰ :幼兔 ,单纯灌注 30min ;组Ⅱ :幼兔 ,停搏 6 0min ,再灌注 30min。组Ⅲ、组Ⅳ为成兔 ,处理分别同组Ⅰ、组Ⅱ ,进行对照。测定各组心功能、冠状动脉流出液血气 ,单细胞内游离钙离子浓度 ([Ca2 + ]i) ,肌浆网Ca2 + -ATPase活性 ,肌浆网45Ca2 + 摄取。结果 :缺血 -再灌注后 ,成熟与未成熟心肌均发生钙超载 (P >0 .0 5 )。未成熟心肌肌浆网Ca2 + ATPase活性 ,肌浆网45Ca2 + 摄取恢复率 ,明显高于成熟心肌 (P <0 .0 5 )。结论 :未成熟心肌缺血 -再灌注损伤钙超载机制不同于成熟心肌 ,肌浆网钙摄取功能 ,在钙超载损伤中不起主要作用。
Objective: To study the calcium function of sarcoplasmic reticulum (SR) in immature myocardial ischemia-reperfusion injury at subcellular level. Methods: Thirty - six rabbits were randomly divided into 4 groups and were perfused with isolated heart. Group Ⅰ: young rabbits, simple perfusion 30min; Group Ⅱ: young rabbits, arrest 60min, reperfusion 30min. Group Ⅲ, Ⅳ into rabbits, respectively, with the same group Ⅰ, Ⅱ, control. The cardiac function, coronary effluent blood gas, single intracellular free calcium concentration ([Ca2 +] i), sarcoplasmic reticulum Ca2 + -ATPase activity and sarcoplasmic reticulum 45Ca2 + uptake were determined. Results: After ischemia-reperfusion, calcium overload occurred in both mature and immature myocardium (P> 0.05). Immature myocardial sarcoplasmic reticulum Ca2 + ATPase activity, sarcoplasmic reticulum 45Ca2 + recovery rate was significantly higher than that of mature myocardium (P <0.05). CONCLUSION: The mechanism of calcium overload in immature myocardial ischemia-reperfusion injury is different from that of mature myocardium and sarcoplasmic reticulum calcium uptake and can not play a major role in calcium overload injury.